Fonberg E, Korczyński R
Nencki Institute of Experimental Biology, Department of Neurophysiology, Warsaw, Poland.
Integr Physiol Behav Sci. 1993 Apr-Jun;28(2):118-29. doi: 10.1007/BF02691214.
Experiments were performed on dogs with bilateral electrolytic damage of dorso-medial amygdala. Before the operation dogs were trained in alimentary-social reward differentiation. It consisted in conditioning of instrumental responses of either right or left foreleg to two different tones respectively. Chlorpromazine was injected intramuscularly in 1.5 mg/kg dose during four consecutive days, beginning at third to fifth week after the operation. Amygdala damage produced significant deterioration of the instrumental performance both reinforced by food and by social-sensory rewards. Chlorpromazine produced further dramatic decrease of performance of both responses. It was concluded that chlorpromazine exerts a suppressing effect on motivated behavior reinforced by positive rewards in amygdala dogs. As the effect of chlorpromazine and medial amygdalar damage are summated it may be suggested that the deficit of medial amygdala neurons impairs similar neurochemical mechanisms, (probably dopaminergic and alpha-adrenergic transmission) as does chlorpromazine.
对双侧背内侧杏仁核遭受电解损伤的狗进行了实验。手术前,狗接受了食物 - 社交奖励辨别训练。训练内容包括分别将右前肢或左前肢的工具性反应条件化至两种不同音调。在手术后第三至第五周开始,连续四天以1.5毫克/千克的剂量肌肉注射氯丙嗪。杏仁核损伤导致由食物和社交感觉奖励强化的工具性表现显著恶化。氯丙嗪使两种反应的表现进一步急剧下降。得出的结论是,氯丙嗪对杏仁核损伤的狗中由积极奖励强化的动机行为具有抑制作用。由于氯丙嗪和内侧杏仁核损伤的作用是累加的,因此可以推测内侧杏仁核神经元的缺陷损害了与氯丙嗪类似的神经化学机制(可能是多巴胺能和α - 肾上腺素能传递)。